To study the effect of basic dispersion of refractoriness on the premature dispersion and propensity to ventricular arrhythmias, an open-chest dog preparation was developed in our laboratory. Graded dispersion with only slight depression of conduction is produced by mild generalized hypothermia (28-29 degrees C) and regiona warm blood perfusion (38-39 degrees C) through distal left anterior descending coronary artery. Ventricular premature stimuli scanning diastole at 10 msec intervals are delivered up to refractoriness to a 40 mA stimulus. Dispersion is measured as the difference between the ends of six simultaneously recorded monophasic action potentials (MAP) and sequence of activation computed using 8-12 critically placed plunge electrodes. The measured dispersion is analyzed in terms of conduction dispersion and MAP duration dispersion. The maximum premature dispersion is related to its position on the strength-interval curve. Changes in premature MAP duration are related to the proximity to the repolarization of the basic MAP. The purpose of our experiments is to increase our understanding of the mechanism of those arrhythmias which are predominantly dependent on increased dispersion of refractoriness. Effects of pharmacologic interventions on the characteristics and the consequences of dispersion will be tested.